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AQA Psychology A Level Schizophrenia 16 Mark Essay Plans

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AQA A-Level Psychology Schizophrenia – ALL 16-Mark Essay Plans (A*) This resource contains all AQA A-Level Psychology Schizophrenia 16-mark essay plans, written by an A* Psychology student. Teacher-marked and awarded top-band marks (14–16/16) Covers all key AO1 and AO3 points required for top-band answers Structured to meet AQA mark-scheme requirements These essay plans were the primary resource used to achieve an A* in A-Level Psychology and are ideal for students aiming to secure consistent top-band marks in 16-mark essays. This includes essay plans for: - Discuss the Biological Explanations of Schizophrenia - Discuss Biological Therapies for Schizophrenia - Discuss issues with reliability and validity associated with classifying and diagnosing schizophrenia. - Discuss Psychological Explanations for Schizophrenia - Discuss Psychological Therapies for Schizophrenia - Discuss Token Economies as a Method to Manage Schizophrenia

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Discuss the Biological Explanations of Schizophrenia

AO1 Dopamine Hypothesis:
- The original dopamine hypothesis stated that schizophrenia was caused by
excess dopamine in the subcortical areas of the brain. However, updated
versions have stated low DA in the prefrontal cortex leads to negative
symptoms such as avolition whereas excess dopamine in the brain leads to
positive symptoms such as hallucinations.

Genetics:
- Family studies have confirmed that the risk of schizophrenia increases in
line with the genetic similarity of the relative with the condition. This is
supported by Gottesman who found that someone with an aunt with
schizophrenia has a 2% chance of developing it, with a sibling increases the
chance to 9% and with a MZ twin, increases the chance to 48%
- From this research, psychologists found that schizophrenia is polygenetic
and that schizophrenic genes would code for differences in dopamine.
- Schizophrenia can also have genetic basis even if there is no family history
of it. This is because genes can mutate to become schizogenesis. Evidence
for mutation comes from the positive correlations between paternal age
and the risk of schizophrenia increasing. This is because the increase in
age, increases the risk of mutation.
AO3 1. Further research support for the genetic basis of schizophrenia is from
Tienari et al who conducted an adoption study which showed that
adopted children into stressful homes with biological mothers with
schizophrenia were more likely to develop schizophrenia than adopted
children into stressful homes without schizophrenic mothers. Showing
genetics plays a greater role in the development of schizophrenia than
environment.
2. Biologically reductionist- this approach only takes into consideration
the effects of biology and no other factors such as the environment.
Furthermore, by separating biological and environmental influences
which could be combined in the development of schizophrenia, this
decreases the validity of the explanation. Hence why an interactionist
approach may be better at explaining schizophrenia, as it takes into
account both influences.
3. Biologically deterministic- this approach implies that if someone has
the genes or low dopamine, they are destined to develop schizophrenia
and it cannot be cured. However, this is not the case as we know some
people may have the genes, but they may not be expressed so therefore
the person won’t develop schizophrenia. Furthermore, it could leave
people feeling hopeless about recovery and lead to difficulties in
treatment when we know that treatments can significantly improve the
quality of life of sufferers.
4. Implications into drug treatment- because we know that
schizophrenia is caused by excess dopamine, drugs such as
antipsychotics can be used to reduce dopamine levels and therefore
reduce schizophrenia symptoms such as hallucinations.
5. Twin studies have provided evidence for the genetic basis of
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